We have also identified the following: three distinct clusters which are more prevalent in LS subjects compared with controls, one of which supports a myofibroblast-like identity; clusters that overlap in expression with identified SSc clusters, while others are unique to LS; an unexpected general inflammatory gene expression in LS fibroblasts (IFN- and HLA-related) compared with healthy fibroblasts; and potential roles for fibroblasts through cell–cell communication and trajectory software, especially macrophage interaction. Here, IFNA1 is linked to Leigh syndrome.